Abstract
Vascular calcification (VC) has witnessed a surge of interest. Vasculature is virtually an omnipresent organ and has a notably high capacity for repair throughout embryonic and adult life. Of the vascular diseases, atherosclerosis is a leading cause of morbidity and mortality on account of ectopic cartilage and bone formation. Despite the identification of a number of risk factors, all the current theories explaining pathogenesis of VC in atherosclerosis are far from complete. The most widely accepted response to injury theory and smooth muscle transdifferentiation to explain the VC observed in atherosclerosis is being challenged. Recent focus on circulating and resident progenitor cells in the vasculature and their role in atherogenesis and VC has been the driving force behind this review. This review discusses intrinsic cellular players contributing to fate determination of cells and tissues to form ectopic cartilage and bone formation.
Highlights
Vascular calcification (VC) is an important complication of atherosclerosis contributing to cardiovascular morbidity and mortality (Alexopoulos and Raggi, 2009), given the increased risk of heart attack with calcified coronaries and the growing incidence of calcified aortic stenosis (Rajamannan et al, 2007)
The most recent concept is that VC is an active, organized, complex, and highly regulated process reflecting the plasticity of vasculature (Bostrom, 2016)
This review focuses on different resident and circulating cells that play a role in ectopic cartilage and bone formation in the vessel wall
Summary
Vascular calcification (VC) is an important complication of atherosclerosis contributing to cardiovascular morbidity and mortality (Alexopoulos and Raggi, 2009), given the increased risk of heart attack with calcified coronaries and the growing incidence of calcified aortic stenosis (Rajamannan et al, 2007). Calcification of atherosclerotic plaque recapitulates virtually the same biologic reactions inherent to normal physiologic bone formation (Neven and D’Haese, 2011). This recapitulation is evidenced by the presence of bone-like structures in the atherosclerotic arteries and valves, which in many cases is structurally complete trabecular bone (Hunt et al, 2002). This resemblance is not just at the macroscopic level but even at microscopic level shows features such as completely formed marrow cavities with hematopoietic and marrow stromal cells (Bunting, 1906; Soor et al, 2008). This review focuses on different resident and circulating cells that play a role in ectopic cartilage and bone formation in the vessel wall
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